ArticleBMC microbiology2025
Uropathogenic Escherichia coli (UPEC) that hides its identity: features of LC2 and EC73 strains from recurrent urinary tract infections.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Double agent: how Escherichia coli switches from commensal to pathogen in the urinary tract infection.Infection · 2026Review
- Mechanisms Linking Recurrent Bacterial Urinary Tract Infections to Chronic Kidney Disease Progression.International journal of molecular sciences · 2026Review
- Prophylactic Potential ofMicroorganisms · 2026Article
- Biophysical Features of Outer Membrane Vesicles (OMVs) from PathogenicAntibiotics (Basel, Switzerland) · 2026Article
- Epitranscriptomic control of stress adaptations in Escherichia coli.Nucleic acids research · 2026Article
- More than an infection: the ecological puzzle of recurrent urinary tract infections.Frontiers in cellular and infection microbiology · 2026Review
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Authors and funding
15 authors.
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Abstract
backgroundUropathogenic Escherichia coli (UPEC) strains are the major causative agents of human urinary tract infections (UTIs). Many patients who develop UTIs will experience a recurrent UTI (RUTI) within 6 months despite antibiotic-mediated clearance of the initial infection. A significant proportion of RUTIs are caused by E. coli identical to the original strain. UPEC employs several strategies to adhere, colonize, and persist within the bladder niche. Knowledge about the mechanisms regulating specific host-pathogen interactions that promote bacterial persistence is necessary to develop new approaches to RUTI diagnosis and treatment.
resultsLC2 and EC73 UPEC strains were collected from patients with RUTIs. E. coli CFT073 and K-12 MG1655 were used as reference strains. UPEC displayed phenotypic profiles like those of the general E. coli population. The pan-genome analysis revealed that LC2 harbored many unique genes encoding several different functions such as intracellular trafficking and secretion, and vesicular transport. Contrarily, EC73 was the strain with the lowest number of unique genes involved in replication, recombination, repair and cell wall/membrane/envelope biogenesis. LC2 and EC73 exhibited the capacity to invade bladder monolayers efficiently and to colonize the gut of Caenorhabditis elegans, with LC2 being significantly more virulent than EC73. T24 cells infected with EC73 and LC2 strains exhibited significantly increased mRNA levels of IL-6, IL-8, IL-1β and TNF-α. EC73 elicited the strongest cytokine response. Differently, no significant cytokine mRNA induction was detected in T24 cells infected with E. coli CFT073. LC2 and EC73 modulated the expression of proteins involved in reactive oxygen species (ROS) balance in infected cells, but to different extents.
conclusionThe acquisition of virulence factors by horizontal transfer of accessory DNA, other than being the cause of transformation to pathogenic strains, is responsible for the genomic plasticity. Our findings suggest that a key role in RUTIs could be played by certain bacterial strains that may benefit from peculiar abilities to adapt and potentially develop reservoirs of persistence across different host environments.
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